|
KMID : 1034820150110010047
|
|
Molecular & Cellular Toxicology
2015 Volume.11 No. 1 p.47 ~ p.53
|
|
|
CIC-3 chloride channel blockade protects mouse photoreceptor-derived 661W cells against ischemia-reperfusion-induced injury in vitro
|
|
Huang Shi Wei
Yin Yuan
Zheng Ya Juan
Dong Ya Ru
|
|
|
Abstract
|
|
|
|
Exposure to ischemia/reperfusion leads to the development and progression of retinal degenerative diseases. However, the exact mechanisms are not fully understood. In this article, the role of CIC-3 chloride channel in OGD-R (oxygen-glucose deprivation followed by reperfusion)-induced retinal damage was examined. Mouse photoreceptor-derived 661W cells were treated with the CIC-3 antisense oligonucleotide before exposure to OGD-R. Cell viability, mitochondrial membrane potential, cytochrome-c level, DNA fragmentation, caspase activity and protein expression were detected. Pretreatment of 661W cells with CIC-3 antisense oligonucleotide significantly decreased OGD-R-mediated toxicity. In addition, apoptosis-related biochemical indicators showed that pre-incubation of CIC-3 antisense oligonucleotide would elevate the mitochondrial membrane potential, decrease the release of cytochrome-c as well as formation of DNA fragmentation, and inhibit activities of caspase-3 and caspase- 9 in exogenous OGD-R-treated 661W cells. Moreover, treatment with CIC-3 antisense oligonucleotide changed the expression of apoptosis-related protein. These results suggest that CIC-3 chloride channel mediates OGD-R-induced apoptosis, at least partially through mitochondrial membrane potential pathway and increasing the levels of proapoptotic molecules in 661W cells. CIC-3 chloride channel blockade may provide a new therapeutic approach for preventing ischemia/reperfusion-induced retinal neural damage.
|
|
|
KEYWORD
|
|
|
CIC-3 chloride channels, 661W cells, Oxygen-glucose deprivation /reperfusion, Antisense oligonucleatide
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|
|